What is the Role of 177Lu-PSMA-617 in Metastatic CRPC?


Panelists share insight on 177Lu-PSMA-617 and consider where it might fit into the treatment paradigm for metastatic castration-resistant prostate cancer.


Evan Y. Yu, MD: We still have a big topic to talk about and I'm going to move on to LU-MPSMA-617. I know Mary Ellen, you know this topic quite well.

Mary-Ellen Taplin, MD: I do.

Evan Y. Yu, MD: I heard your discussion. Let's talk about the key big trials. Vision, therapy, updates. What are your thoughts on that data, and you want to tell us the latest and greatest?

Mary-Ellen Taplin, MD: People are familiar with the vision trial design. We had an update this morning at an oral abstract session and the data is holding up, looking quite good in all the subsets including overall survival benefit. It remains a very sought after treatment for our patients. We were all about to start to give it standard of care. Novartis had a manufacturing problem and they're just coming out of that. At least in the US [United States] patients will soon be able to obtain this therapy post chemotherapy for MCRPC. A lot of exciting trials going on in this space. Trying to move the treatment up earlier, pre chemotherapy MCRPC. And even for hormone sensitive metastatic prostate cancer. And then multiple combination trials were mentioned with PARP and chemotherapy and others. It's just the beginning quite honestly. There's a lot of opportunity not only for PSMA lutetium 617 but for other compounds that are in development. I still worry that there's a dosing or on-target effect, lack of effect or lack of optimal dosing being seen because it's such a potentially useful treatment in terms of the biomarker, the extent of expression of PSMA at least in the very advanced patients. The difference in overall survival is four months, which is not different from Radium quite frankly. I think either defining the most optimal group of patients, which they've done more due diligence in the Australian trials with selecting patients based on not having a lot of non-PSMA expressing disease.

Evan Y. Yu, MD: They had strict criteria.

Mary-Ellen Taplin, MD: Right. On gallium scan. Their criteria were much stricter than the Vision trial and perhaps the benefit would be better in a smaller group of patients if they were selected differently. I'm excited to have the opportunity for my patients.

Evan Y. Yu, MD: We've seen some of that PET biomarker data from both therapy, GU ASCO, [American Society of Clinical Oncology Genitourinary] and Eduvision. Andy, you presented some of that today. It's basically what you would expect if you expressed more PSMA. I think it was SUV mean. A total body mean. Those patients do better.

Andrew J. Armstrong, MD, MSc: They do.

Evan Y. Yu, MD: What does that mean? Does that mean if you have a lower expresser, you're not going to give Lutetium? If you have a no-expresser that's easy, right? But if you have a low expresser how's that going to affect any of your treatments?

Andrew J. Armstrong, MD, MSc: Thanks for asking that. I wanted to make the point that even the low expresser among the positive patients seem to have a better outcome than a second AR inhibitor. Now if you're choosing between cabazitaxel maybe you need an SUV mean of ten to really beat cabazitaxel. But if your goal is just survival that's one aspect but there's also quality of life and toxicity. A lot of these men are elderly and frail, and they may have been beat up by their prior docetaxel and they don't want cabazitaxel. Cabazitaxel can still be used and it's still a great drug and we use it all the time. But a patient who might be on the dimmer side maybe more-you might shunt them toward cabazitaxel in a very homogeneous bright patient would have a greater benefit from a PSMA targeted therapy.

Transcript edited for clarity.

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